{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rahman MA"],"funding":["Norges Forskningsråd","Kreftforeningen"],"pagination":["1022191"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9814514"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10"],"pubmed_abstract":["<b>Introduction:</b> Glioblastoma (GBM) is invariably resistant to temozolomide (TMZ) chemotherapy. Inhibiting the proteasomal pathway is an emerging strategy to accumulate damaged proteins and inhibit their lysosomal degradation. We hypothesized that pre-treatment of glioblastoma with bortezomib (BTZ) might sensitize glioblastoma to temozolomide by abolishing autophagy survival signals to augment DNA damage and apoptosis. <b>Methods:</b> P3 patient-derived glioblastoma cells, as well as the tumour cell lines U87, HF66, A172, and T98G were investigated for clonogenic survival after single or combined treatment with temozolomide and bortezomib <i>in vitro</i>. We investigated the requirement of functional autophagy machinery by utilizing pharmacological inhibitors or CRISPR-Cas9 knockout (K"],"journal":["Frontiers in cell and developmental biology"],"pubmed_title":["Bortezomib abrogates temozolomide-induced autophagic flux through an ATG5 dependent pathway."],"pmcid":["PMC9814514"],"funding_grant_id":["230691 221831","6786380 171318"],"pubmed_authors":["Birkeland E","Goplen D","Simonsen A","Bindesboll C","Rahman MA","Engelsen AST","Sarowar S","Lotsberg ML","Knappskog S","Chekenya M"],"additional_accession":[]},"is_claimable":false,"name":"Bortezomib abrogates temozolomide-induced autophagic flux through an ATG5 dependent pathway.","description":"<b>Introduction:</b> Glioblastoma (GBM) is invariably resistant to temozolomide (TMZ) chemotherapy. Inhibiting the proteasomal pathway is an emerging strategy to accumulate damaged proteins and inhibit their lysosomal degradation. We hypothesized that pre-treatment of glioblastoma with bortezomib (BTZ) might sensitize glioblastoma to temozolomide by abolishing autophagy survival signals to augment DNA damage and apoptosis. <b>Methods:</b> P3 patient-derived glioblastoma cells, as well as the tumour cell lines U87, HF66, A172, and T98G were investigated for clonogenic survival after single or combined treatment with temozolomide and bortezomib <i>in vitro</i>. We investigated the requirement of functional autophagy machinery by utilizing pharmacological inhibitors or CRISPR-Cas9 knockout (K","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-05-28T03:44:00.352Z","creation":"2025-04-04T20:20:30.633Z"},"accession":"S-EPMC9814514","cross_references":{"pubmed":["36619857"],"doi":["10.3389/fcell.2022.1022191"]}}